When neurons from a motoneuron pool are subjected to increasing excitatory synaptic input, the resulting patterns of motoneuronal recruitment and rate modulation are usually highly ordered, and bear a near-optimal relation to the contraction speed and fatigability of the innervated muscle fibers. In acute spinal cord injury, these relations appear to break down, so that there is a compression of recruitment range, a substantial reduction in minimum firing rate, and an increase in motoneuron synchrony. The sources of these changes in motoneuron response are not understood. They could be mediated by alterations in the patterns of excitatory and inhibitory interneuronal input to spinal motoneurons (so that smaller motoneurons are relatively inhibited and larger motoneurons are excited), or they could be induced by changes in the intrinsic properties of spinal motoneurons. These changes in intrinsic properties could be mediated by reductions in monoamines released at segmental levels by pathways traversing the lesioned dorsolateral funiculus. To investigate these issues, we will pursue four objectives. First, we will refine the design of a cold-block system, which will reversibly block fiber conduction in dorsal pathways of the cord. We will then determine whether this cold block replicates the changes in motoneuron responses observed in the surgically lesioned cord. Second, using extracellular recordings of motoneuron discharge, we will determine whether monoamine agonists or antagonists modify the response patterns of motoneurons in normal or cold-blocked cords. Third, we will evaluate the intrinsic characteristics and synaptic inputs to spinal motoneurons using intracellular recordings in normal and cold-blocked spinal cord. Fourth, we will examine the effects of intrathecally administered monoamines on cellular responses using intracellular recordings in motoneurons. These studies should materially improve our understanding of the disturbances in segmental function which follow spinal injury, and help rationalize pharmacological intervention in this important disorder. In addition, they should clarify the factors regulating normal neuronal discharge rate, and help specify which properties are legitimately identified as "intrinsic" to the motoneuron.